INTRODUCTION:
The maximal lactate accumulation rate (vLamax), defined as the peak of the instantaneous lactate accumulation rate vLa(t), is widely used as a proxy of anaerobic glycolytic power. Current gold-standard protocols estimate vLamax from net blood lactate accumulation during short maximal sprints of fixed duration (typically 10 to 20 s; commonly 12 s in cycling), implicitly assuming that peak glycolytic flux coincides with the selected test. This assumption has never been experimentally verified and neglects the inherently time-dependent and self-inhibiting nature of glycolysis. The aim of this study was to develop and validate a time-resolved energy-share framework to quantify vLa(t) from a single maximal sprint and to identify the individual peak vLamax and its timing.
METHODS:
17 elite track cyclists performed maximal sprint tests over 12 and 60 s with continuous mechanical power recording. Pulmonary gas exchange (BxB), muscle oxygenation (NIRS), and capillary blood lactate were measured. Total metabolic energy turnover was estimated from mechanical work using a time-varying gross-efficiency model. Aerobic and alactic energy contributions were quantified from gas-exchange kinetics constrained by NIRS, and glycolytic energy was obtained as the residual. From the glycolytic component, cumulative lactate formation and instantaneous vLa(t) were derived; vLamax was defined as max[vLa(t)] and tvLamax as its timing. Outputs were compared to conventional 12 s vLamax estimates.
RESULTS:
All athletes exhibited a distinct unimodal vLa(t) profile with an individual peak at 9.2 +/- 1.1 s. Time-resolved vLamax exceeded gold-standard values by 0.18 +/- 0.09 mmol / L / s (p < 0.001), demonstrating systematic underestimation by fixed-duration protocols. In contrast, cumulative lactate accumulation over 12 s was accurately reproduced (bias 0.02 +/- 0.15 mmol / L), supporting model validity. Peak timing varied markedly between athletes (range 7.1 to 11.4 s) and was significantly associated with optimal cadence and PCr contribution (R2 = 0.526, RMSE = 1.16 s, p = 0.005). The modeled alactic phase duration (talac = 2.55 +/- 0.94 s) did not differ significantly from the time of first deviation from the fatigue-free force-velocity profile (tFF = 2.95 +/- 0.51 s; p = 0.10), indicating close agreement between mechanically derived and metabolically reconstructed estimates of the initial lactate-free phase.
CONCLUSION:
Fixed-duration sprint protocols do not capture true peak glycolytic flux and introduce a systematic methodological bias in vLamax assessment. Time-resolved analysis reveals that maximal glycolytic activation occurs earlier and within a narrow, individual window. Identification of the alactic phase alone is insufficient when peak glycolytic flux precedes the predefined test duration. Individualized sprint durations based on peak timing could improve the validity of anaerobic tests and challenges the continued use of non-individualized fixed-duration vLamax testing in high-performance sport.